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Hypoxia modulation of peroxisome proliferator-activated receptors (PPARs) in human glioblastoma stem cells. Implications for therapy
Gliobastoma (GB), the most common adult brain tumor, infiltrates normal brain area rendering impossible the complete surgical resection, resulting in a poor median survival (14–15 months), despite the aggressive multimodality treatments post‐surgery, such as radiation and chemo‐therapy. GB is charac...
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| Published in: | Journal of cellular biochemistry 2012-11, Vol.113 (11), p.3342-3352 |
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| container_end_page | 3352 |
| container_issue | 11 |
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| container_title | Journal of cellular biochemistry |
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| creator | Galzio, Renato Cristiano, Loredana Fidoamore, Alessia Cifone, Maria Grazia Benedetti, Elisabetta Cinque, Benedetta Menghini, Paola Raysi Dehcordi, Sohelia Ippoliti, Rodolfo Giordano, Antonio Cimini, Annamaria |
| description | Gliobastoma (GB), the most common adult brain tumor, infiltrates normal brain area rendering impossible the complete surgical resection, resulting in a poor median survival (14–15 months), despite the aggressive multimodality treatments post‐surgery, such as radiation and chemo‐therapy. GB is characterized by hypoxic and necrotic regions due to a poorly organized tumor vascularization, leading to inadequate blood supply and consequently to hypoxic and necrotic areas. We have previously shown that, under hypoxia GB primary cells increased the expression of stemness markers as well as the expression of the nuclear receptor peroxisome proliferator‐activated receptor α (PPARα) and also the crucial role played by PPARs in mouse neural stem cells maintenance and differentiation. Due to the importance of lipid signaling in cell proliferation and differentiation, in this work, we analyzed the expression of PPARs in GB neurospheres both in normoxic and hypoxic conditions. The results obtained suggest a differential regulation of the three PPARs by hypoxia, thus indicating a possible therapeutic strategy to counteract GB recurrencies. J. Cell. Biochem. 113: 3342–3352, 2012. © 2012 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/jcb.24210 |
| format | article |
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Implications for therapy</title><source>Wiley-Blackwell Read & Publish Collection</source><creator>Galzio, Renato ; Cristiano, Loredana ; Fidoamore, Alessia ; Cifone, Maria Grazia ; Benedetti, Elisabetta ; Cinque, Benedetta ; Menghini, Paola ; Raysi Dehcordi, Sohelia ; Ippoliti, Rodolfo ; Giordano, Antonio ; Cimini, Annamaria</creator><creatorcontrib>Galzio, Renato ; Cristiano, Loredana ; Fidoamore, Alessia ; Cifone, Maria Grazia ; Benedetti, Elisabetta ; Cinque, Benedetta ; Menghini, Paola ; Raysi Dehcordi, Sohelia ; Ippoliti, Rodolfo ; Giordano, Antonio ; Cimini, Annamaria</creatorcontrib><description>Gliobastoma (GB), the most common adult brain tumor, infiltrates normal brain area rendering impossible the complete surgical resection, resulting in a poor median survival (14–15 months), despite the aggressive multimodality treatments post‐surgery, such as radiation and chemo‐therapy. GB is characterized by hypoxic and necrotic regions due to a poorly organized tumor vascularization, leading to inadequate blood supply and consequently to hypoxic and necrotic areas. We have previously shown that, under hypoxia GB primary cells increased the expression of stemness markers as well as the expression of the nuclear receptor peroxisome proliferator‐activated receptor α (PPARα) and also the crucial role played by PPARs in mouse neural stem cells maintenance and differentiation. Due to the importance of lipid signaling in cell proliferation and differentiation, in this work, we analyzed the expression of PPARs in GB neurospheres both in normoxic and hypoxic conditions. The results obtained suggest a differential regulation of the three PPARs by hypoxia, thus indicating a possible therapeutic strategy to counteract GB recurrencies. J. Cell. Biochem. 113: 3342–3352, 2012. © 2012 Wiley Periodicals, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.24210</identifier><identifier>PMID: 22644833</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Biomarkers - metabolism ; Blotting, Western ; Brain Neoplasms - genetics ; Brain Neoplasms - metabolism ; Brain Neoplasms - pathology ; Cell Hypoxia ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cholesterol - metabolism ; Gene Expression Regulation, Neoplastic - drug effects ; Glioblastoma - genetics ; Glioblastoma - metabolism ; Glioblastoma - pathology ; GLIOBLASTOMA STEM CELLS ; Humans ; HYPOXIA ; Microscopy, Fluorescence ; Neoplastic Stem Cells - drug effects ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - pathology ; Oxygen - pharmacology ; PPAR alpha - genetics ; PPAR alpha - metabolism ; PPAR gamma - genetics ; PPAR gamma - metabolism ; PPAR-beta - genetics ; PPAR-beta - metabolism ; PPARs ; Signal Transduction</subject><ispartof>Journal of cellular biochemistry, 2012-11, Vol.113 (11), p.3342-3352</ispartof><rights>Copyright © 2012 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4900-67fddba900c37e9ebfe94a9663ff96052be119cbd8a94023ad1560bf36c782c93</citedby><cites>FETCH-LOGICAL-c4900-67fddba900c37e9ebfe94a9663ff96052be119cbd8a94023ad1560bf36c782c93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22644833$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Galzio, Renato</creatorcontrib><creatorcontrib>Cristiano, Loredana</creatorcontrib><creatorcontrib>Fidoamore, Alessia</creatorcontrib><creatorcontrib>Cifone, Maria Grazia</creatorcontrib><creatorcontrib>Benedetti, Elisabetta</creatorcontrib><creatorcontrib>Cinque, Benedetta</creatorcontrib><creatorcontrib>Menghini, Paola</creatorcontrib><creatorcontrib>Raysi Dehcordi, Sohelia</creatorcontrib><creatorcontrib>Ippoliti, Rodolfo</creatorcontrib><creatorcontrib>Giordano, Antonio</creatorcontrib><creatorcontrib>Cimini, Annamaria</creatorcontrib><title>Hypoxia modulation of peroxisome proliferator-activated receptors (PPARs) in human glioblastoma stem cells. Implications for therapy</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>Gliobastoma (GB), the most common adult brain tumor, infiltrates normal brain area rendering impossible the complete surgical resection, resulting in a poor median survival (14–15 months), despite the aggressive multimodality treatments post‐surgery, such as radiation and chemo‐therapy. GB is characterized by hypoxic and necrotic regions due to a poorly organized tumor vascularization, leading to inadequate blood supply and consequently to hypoxic and necrotic areas. We have previously shown that, under hypoxia GB primary cells increased the expression of stemness markers as well as the expression of the nuclear receptor peroxisome proliferator‐activated receptor α (PPARα) and also the crucial role played by PPARs in mouse neural stem cells maintenance and differentiation. Due to the importance of lipid signaling in cell proliferation and differentiation, in this work, we analyzed the expression of PPARs in GB neurospheres both in normoxic and hypoxic conditions. The results obtained suggest a differential regulation of the three PPARs by hypoxia, thus indicating a possible therapeutic strategy to counteract GB recurrencies. J. Cell. Biochem. 113: 3342–3352, 2012. © 2012 Wiley Periodicals, Inc.</description><subject>Biomarkers - metabolism</subject><subject>Blotting, Western</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - metabolism</subject><subject>Brain Neoplasms - pathology</subject><subject>Cell Hypoxia</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cholesterol - metabolism</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Glioblastoma - genetics</subject><subject>Glioblastoma - metabolism</subject><subject>Glioblastoma - pathology</subject><subject>GLIOBLASTOMA STEM CELLS</subject><subject>Humans</subject><subject>HYPOXIA</subject><subject>Microscopy, Fluorescence</subject><subject>Neoplastic Stem Cells - drug effects</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Oxygen - pharmacology</subject><subject>PPAR alpha - genetics</subject><subject>PPAR alpha - metabolism</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>PPAR-beta - genetics</subject><subject>PPAR-beta - metabolism</subject><subject>PPARs</subject><subject>Signal Transduction</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNqFkU9vFCEYh4nR2G314BcwJF7aw2z5N8NybDfa1mzqRms8EoYBywrDCDO2e_eDS7ttDybGE-TN8z68Lz8A3mA0xwiR441u54QRjJ6BGUaCV6xh7DmYIU5RRSgme2A_5w1CSAhKXoI9QgqwoHQGfp9vh3jrFAyxm7waXexhtHAwqVRzDAYOKXpnTVJjTJXSo_ulRtPBZLQZSinDw_X65HM-gq6H11NQPfzuXWy9ymMMCubRBKiN93kOL8Lgnb5_JEMbExyvi3fYvgIvrPLZvH44D8DXD--vlufV6tPZxfJkVWkmEKoabruuVeWqKTfCtNYIpkTTUGtFg2rSGoyFbruFEgwRqjpcN6i1tNF8QbSgB-Bw5y07_ZxMHmVw-W421Zs4ZYkZFaR8I2f_RxHDlNSoXhT03V_oJk6pL4vIghBGuaC0UEc7SqeYczJWDskFlbZFJe9SlCVFeZ9iYd8-GKc2mO6JfIytAMc74MZ5s_23SX5cnj4qq12HK4HcPnWo9EM2nPJafrs8k2R9KfjVl5Vc0j9h1bZZ</recordid><startdate>201211</startdate><enddate>201211</enddate><creator>Galzio, Renato</creator><creator>Cristiano, Loredana</creator><creator>Fidoamore, Alessia</creator><creator>Cifone, Maria Grazia</creator><creator>Benedetti, Elisabetta</creator><creator>Cinque, Benedetta</creator><creator>Menghini, Paola</creator><creator>Raysi Dehcordi, Sohelia</creator><creator>Ippoliti, Rodolfo</creator><creator>Giordano, Antonio</creator><creator>Cimini, Annamaria</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201211</creationdate><title>Hypoxia modulation of peroxisome proliferator-activated receptors (PPARs) in human glioblastoma stem cells. 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We have previously shown that, under hypoxia GB primary cells increased the expression of stemness markers as well as the expression of the nuclear receptor peroxisome proliferator‐activated receptor α (PPARα) and also the crucial role played by PPARs in mouse neural stem cells maintenance and differentiation. Due to the importance of lipid signaling in cell proliferation and differentiation, in this work, we analyzed the expression of PPARs in GB neurospheres both in normoxic and hypoxic conditions. The results obtained suggest a differential regulation of the three PPARs by hypoxia, thus indicating a possible therapeutic strategy to counteract GB recurrencies. J. Cell. Biochem. 113: 3342–3352, 2012. © 2012 Wiley Periodicals, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>22644833</pmid><doi>10.1002/jcb.24210</doi><tpages>11</tpages></addata></record> |
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| subjects | Biomarkers - metabolism Blotting, Western Brain Neoplasms - genetics Brain Neoplasms - metabolism Brain Neoplasms - pathology Cell Hypoxia Cell Line, Tumor Cell Proliferation - drug effects Cholesterol - metabolism Gene Expression Regulation, Neoplastic - drug effects Glioblastoma - genetics Glioblastoma - metabolism Glioblastoma - pathology GLIOBLASTOMA STEM CELLS Humans HYPOXIA Microscopy, Fluorescence Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Oxygen - pharmacology PPAR alpha - genetics PPAR alpha - metabolism PPAR gamma - genetics PPAR gamma - metabolism PPAR-beta - genetics PPAR-beta - metabolism PPARs Signal Transduction |
| title | Hypoxia modulation of peroxisome proliferator-activated receptors (PPARs) in human glioblastoma stem cells. Implications for therapy |
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